ELECTROLYTE DISTURBANCE / IMBALANCE

Electrolytes
Are chemicals in the body that regulate important physiological functions-----help to
regulate myocardial and neurological function, fluid balance, oxygen delivery, acid-base
balance .
ELECTROLYTE include sodium, chloride, magnesium, potassium and calcium.
When dissolved in water, electrolytes separate into positively and negatively charged
ions.
Nerve and muscle function are dependent upon the proper exchange of these ions in
and out of the cells.

Electrolytes must exist in the body within a narrow concentration range in order to
effectively serve a variety of critical functions .
The most serious electrolyte disturbances involve abnormalities in
the levels of sodium, potassium, and/or calcium.
Other electrolyte imbalances are less common, and often occur in
conjunction with major electrolyte changes.

Chronic laxative abuse or severe diarrhea or vomiting can lead to

electrolyte disturbances alone or with dehydration.
People suffering from bulimia or anorexia are at especially high
risk for an electrolyte imbalance.
Electrolyte Functions in the body  Normal adult range*
Necessary for muscle  4.5-5.5 mEq/L
Calcium contraction, nerve function,
blood clotting, cell division,
healthy bones and teeth

Chlorida
Maintains fluid balance in the  97-107 mEq/L
body

 3.5-5.3 mEq/L
Potassium Regulates heart contraction,
helps maintain fluid balance

Magnesium  1.5-2.5 mEq/L

Necessary for muscle
contraction, nerve function,
heart rhythm, bone strength,
generating energy and building
protein

Sodium Maintains fluid balance and  136-145 mEq/L

necessary for muscle contraction
and nerve function
Causes electrolyte imbalance
Electrolyte imbalance is commonly caused by
1. loss of body fluids through prolonged vomiting, diarrhea,
sweating, or high fever.
2.side effects of chemotherapy treatment.
3. renal failure.
The kidneys play a critical role in regulating electrolytes.
They control the levels of chloride in the blood and “flush out”
potassium, magnesium and sodium.
Therefore, a disturbance in blood levels of these electrolytes may
be related to kidney function.
Symptoms of electrolyte imbalance
Symptoms that depend on which electrolyte is out of balance and whether the
level is too high or too low.
Altered potassium, magnesium, sodium or calcium levels, can lead one or more
of the following symptoms:
Muscle spasm
Bone disorders
Weakness
Blood pressure changes
Twitching
Irregular heartbeat
Numbness
Nervous system disorders
Confusion
Convulsions
Lethargy
Seizures etc
1. SODIUM
HYPERNATREMIA
Hypernatremia is a greater than normal concentration of sodium in the blood.
Sodium is an electrolyte that helps with nerve and muscle function, and also
helps to maintain blood pressure.

Sodium helps the kidneys to regulate the amount of water the body retains or
excretes.
Consequently, individuals with elevated serum sodium levels also suffer from
a loss of fluids, or dehydration.
CAUSES :
- Inadequate water intake
- Excessive fluid loss ( diabetes insipidus, kidney disease, severe burns, and
prolonged vomiting or diarrhea)
- Sodium retention (caused by excessive sodium intake or aldosteronism).
- Certain drugs, including loop diuretics, corticosteroids, and
antihypertensive medications may cause elevated sodium levels.
Symptoms :
thirst , orthostatic hypotension , dry mouth and mucous membranes
concentrated urine
loss of elasticity in the skin
irregular heartbeat (tachycardia)
irritability
fatigue
lethargy
muscle twitching and/or seizures

Who gets it?

1. Eldery : who may not recognize that they are thirsty or are unable to get
themselves something to drink.
2.Diuretic user : which cause the kidneys to excrete more water
3.Patient diabetes insipidus or diseases of the hypothalamus or pituitary
gland, which can also interfere with normal kidney function.
Diagnose
By measuring the sodium levels in a blood sample.
Normal blood sodium levels are 136 to 145 milliequivalents per liter (mEq/L)
Hypernatremia : blood sodium level higher than 145 mEq/L.
Important: to look for any underlying causes of hypernatremia, such as diabetes
insipidus or other disorders.

Treatment
Principle : replacing the lost fluids.
Mild cases--- drinking electrolyte replacement fluids.
Severe cases--- fluids are given intravenously . The fluid is given slowly, and the
blood sodium levels are constantly monitored so the sodium/water levels are
brought to the proper balance.
Unless brain function has been affected, most people make a full recovery from
hypernatremia.
HYPONATREMIA
Hyponatremia is an electrolyte disturbance in which the sodium (Natrium)
concentration in the plasma below 135 mmol/L

Up to 1% of all hospitalized patients and up to 18% of nursing home patients

develop hyponatremia ---one of the most common electrolyte disorders.
Causes :
1.Excessive IV fluid
Questioned the routine make-up of fluids prescribed for children and delivered
intravenously in hospitals ---recommended only using IV fluids when necessary
and then using isotonic saline.
2.Drug
Diuretics, certain psychoactive drugs (i.e., fluoxetine, sertraline, haloperidol),
specific antipsychotics (lithium), vasopressin, chlorpropamide, “ecstasy," and
other pharmaceuticals can cause decreased sodium levels. "
3.Low intake sodium
Low sodium levels may also be triggered by inadequate dietary intake of sodium,
excessive perspiration, water intoxication, and impairment of adrenal gland or
kidney function.
Symptoms
Most patients with chronic water intoxication are asymptomatic, but may have
symptoms related to the underlying cause.

Severe hyponatremia may cause osmotic shift of water from the plasma into the
brain cells. Typical symptoms include nausea, vomiting, abdominal cramping,
edema (swelling) headache and malaise.

Since nausea is, itself, a stimulus for the release of ADH, which promotes the
retention of water, a positive feedback loop may be created and the potential for a
vicious circle of hyponatremia and its symptoms exists.
As the hyponatremia worsens, confusion, diminished reflexes, convulsions, stupor
or coma may occur.
Causes of hyponatremia
An abnormally low plasma sodium level is best considered in conjunction with
the person's plasma osmolarity and extra cellular fluid volume status.
Most cases of hyponatremia are associated with reduced plasma osmolarity.
Majority of adult cases are due to increased vasopressin, i.e., anti-diuretic
hormone (ADH)--- causes retention of water; salt is also retained but to a lesser
extent. (important to identify the cause of the increased ADH activity in each
case).
Some patients with hyponatremia have normal blood volume.
In those patients, -- nausea --- increased ADH activity / ADH
release ---- water retention ---- hyponatremia : Syndrome of
Inappropriate ADH (SIADH).
Release of ADH some times occurs as a side effect of certain
medicines, lung problems such as pneumonia or abscess, brain
disease, or certain cancers (most often small cell lung carcinoma).
Another condition :
Patients with hyponatremia are often said to be "hypervolemic". They are
identified by the presence of peripheral edema.
In fact, the term "hypervolemic" is misleading since their blood volume is
actually low.
The edema--- fact that fluid has left the circulation--- edema represents fluid
that has exited the circulation and settled in dependent areas.
EDEMA------REDUCE BLOOD VOLUME -----ADH RELEASE-----RETAINED WATER-----
HYPO NATREMIC----- Treatment of these patients involves treating the
underlying disease that caused the fluid to leak out of the circulation in the first
place.
Hyponatremia can also result from adrenal insufficiency, congenital adrenal
hyperplasia, hypothyroidism, and some medication.
Hypoosmolar hyponatremia
When the plasma osmolarity is low, the extracellular fluid volume status may be in one of three
states:

1.Low volume. Loss of water is accompanied by loss of sodium.

Excessive sweating
Burns
Vomiting
Diarrhea
Urinary loss
Diuretic drugs (especially thiazides)
Addison's disease
Cerebral salt-wasting syndrome
Other salt-wasting kidney diseases
Treat underlying cause and give IV isotonic saline.
Be carefull
Sudden restoration of blood volume to normal -----will turn off the stimulus ADH secretion. -----ADH
decrease-----water diuresis will occur -----sudden and dramatic increase the serum sodium
concentration -----place the patient at risk for so-called "central pontine myelinolysis"
(CPM). That disorder is characterized by major neurologic damage, often of a permanent nature.
Because of the risk of CPM, patients with low volume hyponatremia may eventually require water
infusion as well as volume replacement. Doing so lessens the chance of a too rapid increase of the
serum sodium level as blood volume rises and ADH levels fall.
Normal volume.
SIADH (syndrome of inappropriate antidiuretic hormone)
Some cases of psychogenic polydipsia
The cornerstone of therapy for SIADH is reduction of water intake. If hyponatremia persists,
then demeclocycline (an antibiotic with the side effect of inhibiting ADH) can be used.
SIADH can also be treated with specific antagonists of the ADH receptors, such as
conivaptan or tolvaptan.

High volume. There is retention of water.

Congestive heart failure
Hypothyroidism and hypocortisolism
Liver cirrhosis
Nephrotic syndrome
Psychogenic polydipsia
Placing the patient on water restriction can also help in these cases.
2. POTASSIUM
HYPERKALEMIA
Hyperkalemia may be caused by ketoacidosis (diabetic coma), myocardial
infarction (heart attack), severe burns, kidney failure, fasting, bulimia
nervosa, gastrointestinal bleeding, adrenal insufficiency, or Addison's disease.
Diuretic drugs, cyclosporin, lithium, heparin, ACE inhibitors, beta blockers,
and trimethoprim can increase serum potassium levels, as can heavy
exercise.
Symptoms
Nonspecific and generally include malaise, palpitations and muscle
weakness;
During screening blood tests for a medical disorder, or it only comes to
medical attention after complications have developed, such as cardiac
arrhythmia or sudden death.
During the medical history taking, a physician will dwell on kidney disease
and medication use ( as these are the main causes) .

Addison disease :
The combination of abdominal pain, hypoglycemia and hyperpigmentation,
often in the context of a history of other autoimmune disorders.
Diagnosis
Attention : Result increase K in serum can be due to hemolysis in the
sample.

The normal serum level of potassium is 3.5 to 5.3 mEq/L.

Generally, blood tests for renal function (creatinine, blood urea nitrogen), glucose
and occasionally creatine kinase and cortisol will be performed.

In many cases, renal ultrasound will be performed, since hyperkalemia is highly

suggestive of renal failure.
Also, electrocardiography (EKG/ECG) may be performed to determine if there is a
significant risk of cardiac arrhythmias (see ECG/EKG Findings, below).
Causes include:
Ineffective elimination from the body
1. Renal insufficiency
2. Medication that interferes with urinary excretion:
ACE inhibitors and angiotensin receptor blockers
Potassium-sparing diuretics (e.g. amiloride and spironolactone)
NSAIDs such as ibuprofen, naproxen, or celecoxib
The calcineurin inhibitor immunosuppressants ciclosporin and tacrolimus
The antibiotic trimethoprim
The antiparasitic drug pentamidine
3.Mineralocorticoid deficiency or resistance :
Addison's disease
Aldosterone deficiency, including reduced levels due to the blood thinner, heparin
Some forms of congenital adrenal hyperplasia
Type IV renal tubular acidosis (resistance of renal tubules to aldosterone)
 Excessive release from cells
Rhabdomyolysis, burns or any cause of rapid tissue necrosis, including tumor lysis
syndrome
Massive blood transfusion or massive hemolysis
Shifts/transport out of cells caused by acidosis, low insulin levels, beta-blocker therapy,
digoxin overdose, or the paralyzing anesthetic succinylcholine
Excessive intake
Intoxication with salt-substitute, potassium-containing dietary supplements, or potassium
chloride (KCl) infusion. Note that for a person with normal kidney function and nothing
interfering with normal elimination (see above), hyperkalemia by potassium intoxication
would be seen only with large infusions of KCl or massive doses of oral KCl supplements.
Lethal injection
Hyperkalemia is intentionally brought about in an execution by lethal injection, with
potassium chloride being the third and last of the three drugs administered to cause
death..
 PSEUDOHYPERKALEMIA
Pseudohyperkalemia is a rise in the amount of potassium that occurs due to excessive
leakage of potassium from cells, during or after blood is drawn/ take sample for
laboratory examination
Pseudohyperkalemia is typically caused by
1.hemolysis during venipuncture (by either excessive vacuum of the blood draw or by
a collection needle that is of too fine a gauge)
2.excessive tournequet time or fist clenching during phlebotomy (which presumably
leads to efflux of potassium from the muscle cells into the bloodstream); or by a delay
in the processing of the blood specimen.
3.It can also occur in specimens from patients with abnormally high numbers of
platelets (>1,000,000/mm³), leukocytes (> 100 000/mm³), or erythrocytes (hematocrit
> 55%). People with "leakier" cell membranes have been found, whose blood must be
separated immediately to avoid pseudohyperkalemia.[3]
Pathophysiology
Potassium is the most abundant intracellular cation. I
t is critically important for many physiologic processes, including maintenance of cellular
membrane potential, homeostasis of cell volume, and transmission of action potentials in
nerve cells.
Its main dietary sources are vegetables (tomato and potato), fruits (orange and banana)
and meat. Elimination is through the gastrointestinal tract and the kidney.
The renal elimination of potassium is passive (through the glomeruli), and resorption is
active in the proximal tubule and the ascending limb of the loop of Henle. There is active
excretion of potassium in the distal tubule and the collecting duct; both are controlled by
aldosterone.
Hyperkalemia
1.excessive production (oral intake, tissue breakdown) or
2.ineffective elimination of potassium. Ineffective elimination can be hormonal (in
aldosterone deficiency) or due to causes in the renal parenchyma that impair excretion.

Increased extracellular potassium levels result in depolarization of the membrane

potentials of cells. This depolarization opens some voltage-gated sodium channels, but not
enough to generate an action potential. After a short while, the open sodium channels
inactivate and become refractory, increasing the threshold to generate an action potential.
This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems.
Of most concern is the impairment of cardiac conduction which can result in ventricular
fibrillation or asystole.
Treatment
Acute: When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency
lowering of potassium levels is mandated.
Several agents are used to lower K levels. Choice depends on the degree and cause of the
hyperkalemia, and other aspects of the patient's condition.
Calcium supplementation (calcium gluconate 10% (10ml), preferably through a central
venous catheter as the calcium may cause phlebitis) does not lower potassium but
decreases myocardial excitability, protecting against life threatening arrhythmias.
Insulin (e.g. intravenous injection of 10-15u of regular insulin {along with 50ml of 50%
dextrose to prevent hypoglycemia}) will lead to a shift of potassium ions into cells,
secondary to increased activity of the sodium-potassium ATPase.
Bicarbonate therapy (e.g. 1 ampule (45mEq) infused over 5 minutes) is effective in cases
of metabolic acidosis. The bicarbonate ion will stimulate an exchange of cellular H+ for
Na+, thus leading to stimulation of the sodium-potassium ATPase.
Salbutamol (albuterol, Ventolin) is a β2-selective catecholamine that is administered by
nebulizer (e.g. 10-20 mg). This drug promotes movement of K into cells, lowering the
blood levels.
Refractory or severe cases may need dialysis to remove the potassium from the
circulation.
HYPOKALEMIA
Principal causes of potassium depletion.
1. Severe dehydration (cause :Cushing's syndrome, kidney disease, long-term diuretic
therapy)
2.Drug : certain penicillins, laxative abuse,
3. Deficient dietary intake
4.Excessive losses
A.Gastrointestinal
a.Protracted vomiting
b.Diarrhea
c.Fistula
d.Laxative abuse
B..Renal
a. metabolic alkalosis
b.Diuretics
c.Aldosteronism
d.Tubular dysfunction
A major cause of potassium depletion is diuretic use.
Diuretics that block sodium reabsorption in the renal tubule at site proximal to
where sodium – potassium exchange occurs.

The symptoms and signs of potassium depletion usually do not appear until
deficiency is marked.
Determination of plasma potassium is the most valuable aid in the
diagnosis of potassium depletion .
When hypokalemia is present and before any therapy is given,
the urinary potassium concentration is helpful in defining the
etiology of depletion.
If the urine potassium is less than 10 mEq/L , non renal losses
should be defining the etiology of depletion .
When urine potassium concentrations exceeds 10 mEq/L,
depletion is probably secondary to renal losses.
In summary , potassium depletion may be suggested by :
1.Recognition of causative events.
2.Symptoms and signs of neuromuscular dysfunction
3.electrocardiographic changes.
Symptoms
Symptoms of hypokalemia include irregular heartbeat, which can range from
mild to severe.
Severe cases can result in cardiac arrest and paralysis of the lungs.
Other symptoms can include muscle weakness, cramping, or flaccid paralysis
(limpness); leg discomfort; extreme thirst; frequent urination; and confusion.

Infants and young children with gastrointestinal illnesses that cause prolonged
vomiting and diarrhea can die from cardiac arrest when potassium levels
become dangerously low.

Diagnose
Hypokalemia is diagnosed by measuring the potassium levels in a blood sample.
Normal blood potassium levels are 3.5 to 5.3 milliequivalents per liter (mEq/L)
To determine the cause of hypokalemia, --- also check potassium levels in a urine
sample----also order test electrocardiogram (ECG or EKG).

EKG : prominent u waves with flat T

Treatment
Severe hypokalemia : intravenous (IV) potassium.
Mild hypokalemia : treated by increasing the amounts of potassium-rich foods in
the diet, drinking electrolyte replacement fluids during intense exercise or for
severe vomiting or diarrhea, or by taking a potassium supplement .

It is important to have the potassium levels in the blood checked regularly if taking
diuretics or other medications that affect potassium.

Eating a well-balanced diet will prevent low potassium conditions.

It is difficult to predict if hypokalemia will occur with vomiting and diarrhea or

with diuretic use.
CALCIUM
HYPERCALCEMIA
- thyroid disorder
- multiple myeloma
- metastatic cancer
- multiple bone fractures, milk-alkali syndrome, and Paget's disease.
- excessive use of calcium-containing supplements
- certain medications (i.e., antacids)
- in infants, lesser known causes may include blue diaper syndrome, Williams
syndrome, secondary hyperparathyroidism from maternal hypocalcemia, and dietary
phosphate deficiency.
Symptoms include:
fatigue
constipation
depression
confusion
muscle pain
nausea and vomiting
dehydration
increased urination
irregular heartbeat (arrhythmia)
HYPOCALCEMIA
Thyroid disorders, kidney failure, severe burns, sepsis, vitamin D deficiency, and
medications such as heparin and glucagon can deplete blood calcium levels.
Lowered levels cause:
muscle cramps and spasms
tetany and/or convulsions
mood changes (depression, irritability)
dry skin
brittle nails
facial twitching
MAGNESIUM
HYPERMAGNESEMIA
Excessive magnesium levels may occur with end-stage renal disease, Addison's disease, or an
overdose of magnesium salts. Hypermagnesemia is characterized by:
lethargy
hypotension
decreased heart and respiratory rate
muscle weakness
diminished tendon reflexes
HYPOMAGNESEMIA
Inadequate dietary intake of magnesium, often caused by chronic alcoholism or malnutrition, is
a common cause of hypomagnesemia. Other causes include malabsorption syndromes,
pancreatitis, aldosteronism, burns, hyperparathyroidism, digestive system disorders, and
diuretic use. Symptoms of low serum magnesium levels include:
leg and foot cramps
weight loss
vomiting
muscle spasms, twitching, and tremors
seizures
muscle weakness
arrthymia
CHLORIDE
HYPERCHLOREMIA
Severe dehydration, kidney failure, hemodialysis, traumatic brain injury, and
aldosteronism can also cause hyperchloremia. Drugs such as boric acid and
ammonium chloride and the intravenous (IV) infusion of sodium chloride can also
boost chloride levels, resulting in hyperchloremic metabolic acidosis. Symptoms
include:
weakness
headache
nausea
cardiac arrest
HYPOCHLOREMIA
Hypochloremia usually occurs as a result of sodium and potassium depletion (i.e.,
hyponatremia, hypokalemia). Severe depletion of serum chloride levels causes
metabolic alkalosis. This alkalization of the bloodstream is characterized by:
mental confusion
slowed breathing
paralysis
muscle tension or spasm
PHOSPHATE
HYPERPHOSPHATEMIA
Skeletal fractures or disease, kidney failure, hypoparathyroidism, hemodialysis,
diabetic ketoacidosis, acromegaly, systemic infection, and intestinal obstruction can
all cause phosphate retention and build-up in the blood. The disorder occurs
concurrently with hypocalcemia. Individuals with mild hyperphosphatemia are
typically asymptomatic, but signs of severe hyperphosphatemia include:
tingling in hands and fingers
muscle spasms and cramps
convulsions
cardiac arrest
HYPOPHOSPHATEMIA
Serum phosphate levels of 2 mg/dL or below may be caused by hypomagnesemia
and hypokalemia. Severe burns, alcoholism, diabetic ketoacidosis, kidney disease,
hyperparathyroidism, hypothyroidism, Cushing's syndrome, malnutrition,
hemodialysis, vitamin D deficiency, and prolonged diuretic therapy can also diminish
blood phosphate levels. There are typically few physical signs of mild phosphate
depletion. Symptoms of severe hypophosphatemia include:
muscle weakness
weight loss
bone deformities (osteomalacia)
THE END
Background

The serum sodium concentration is regulated by the balance of water intake, renal filtration and
reabsorption of sodium, and antidiuretic hormone (ADH) – mediated water conservation by the
collecting duct. Water balance is normally mediated by thirst, the secretion of antidiuretic hormone
(also known as vasopressin), the feedback mechanisms of the renin-angiotensin-aldosterone system,
and renal handling of filtered sodium and water. Disorders in any one of these components of sodium
balance can result in hyponatremia.1ADH is secreted by supraoptic and paraventricular nuclei in the
hypothalamus and transmitted via the neuronal axons to the posterior pituitary where it is secreted.2 It
is released when a decrease in the effective circulatory volume is sensed by vascular baroreceptors
primarily located in the large arterial vessels. The key action of ADH in the kidney is to trigger the
insertion of aquaporin-2 into the principal cells of the collecting duct. Aquaporins' selective
permeability allows water reabsorption and consequently urine concentration.2

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) was initially described by Leaf
and Mamby. They demonstrated a direct relationship between excessive vasopressin and fall in serum
sodium concentration without any change in urine osmolality or flow rate.3
The key to the pathophysiology, signs, symptoms, and treatment of SIADH is to understand that the
hyponatremia is a result of excess water and not a serum sodium deficiency. SIADH consists of
hyponatremia, inappropriately elevated urine osmolality (>200 mOsm/kg), excessive urine sodium (UNa
>30 mEq/L), and decreased serum osmolality. These findings occur in the absence of diuretic therapy; in
the presence of euvolemia without edema; in the setting of otherwise normal cardiac, renal, adrenal,
hepatic, and thyroid function; and in absence of factors known to stimulate ADH secretion such as severe
pain, hypotension, and stress.

In SIADH, the inappropriately elevated level of vasopressin enhances the reabsorption of water, thus
concentrating the urine. It is the excess free water absorption that causes hyponatremia.

Two scenarios can occur in which vasopressin secretion will be not be correlated with the serum
osmolality. First, a decrease in the effective circulatory volume may be falsely sensed by the large arterial
baroreceptors in conditions such as cirrhosis, nephrotic syndrome, and congestive heart failure. In these
cases, the stimulus for ADH secretion overrides osmotic signals, which are conveying a hypoosmotic state.
ADH secretion ensues despite hypoosmolality resulting in hyponatremia.4 In contrast to patients with
SIADH, these patients appear hypervolemic.

Second, inappropriate ADH secretion occurs when there is dysregulation of cells secreting vasopressin or
in the feedback mechanisms responsible for its release. A variety of ADH-secreting tumors both inside and
outside the pituitary have been associated with SIADH, as well as certain CNS disorders, pulmonary
disorders, and medications (see Differentials).

A distinction should be made between the SIADH and the clinical syndrome of euvolemic hyponatremia. A
mutation of the ADH receptor can make it more responsive to ADH and can result in the same clinical
picture of hyponatremia, concentrated urine output, and decreased serum osmolality but with normal
ADH secretion.5
requency
United States

Hyponatremia is the most common electrolyte derangement occurring in hospitalized patients. When defined as plasma
sodium concentration of less than 135 mEq/L, the prevalence of hyponatremia in hospitalized patients may be as high as 15-
30%.6,7 The prevalence of hyponatremia in hospitalized patients has been reported in different studies as being between 2.5
and 16%.8,6 In a majority of cases, the hyponatremia was found to be hospital acquired. In another study among emergency
department patients, the prevalence of hyponatremia, defined as serum sodium concentration of less than 130 mEq/L, was
2.9%. Additionally, the prevalence of acute hyponatremia was 0.8%.9 Although a number of potential causes of hyponatremia
exist, ADH dysregulation is the most common.8
Mortality/Morbidity

The fatality rate of patients with hyponatremia (sodium <130 mEq/L) is 60-fold compared to that of patients without
documented hyponatremia, though the mortality is typically related to comorbid conditions rather than the hyponatremia
itself. Predictors for higher morbidity and mortality rates include being hospitalized, acute onset, and severe hyponatremia.8

Previously, mild hyponatremia was considered relatively asymptomatic. However, recent evidence suggests that even mild
hyponatremia can cause significant impairment such as unsteady gait and lead to frequent falls. This effect may be greater in
elderly persons who are more sensitive to changes their sodium.10

Race

No evidence for race predilection was found in studies of SIADH.

Sex

Studies reveal variable evidence between gender and hyponatremia. Studies showing that females are at increased risk for
hyponatremia failed to take body mass into account. Men appear to be more likely to get mild or moderate but not severe
hyponatremia.11
Age
Age

Increasing age is a strong risk factor for hyponatremia; although, again, this may be confounded by body mass.11 The very old
and very young develop symptoms with smaller changes in serum sodium levels than adults.12,2
Clinical
History

Signs and symptoms of hyponatremia are primarily related to the central nervous system dysfunction and correlate with
severity and acuity of the hyponatremia. Anorexia, nausea, and malaise are the earliest findings, followed by headache,
irritability, confusion, muscle cramps, weakness, obtundation, seizures, and coma. These occur as osmotic fluid shifts resulting
in cerebral edema and increased intracranial pressure. Those with rapidly decreasing sodium levels manifest more pronounced
symptoms. Patients with moderate chronic hyponatremia may have decreased reaction times, cognitive slowing, and ataxia
resulting in frequent falls.10 When sodium concentration drops below 105 mEq/L, life-threatening complications are likely to
occur.13

Helpful historical details in identifying the responsible mechanism for hyponatremia include diet, fluid intake, gastrointestinal
losses, amount of urinary output, medications, and weight loss. Historical information can give important clues in deciding
whether the hyponatremia is from an acute or chronic condition. This may help the physician in correlating the degree of
hyponatremia with the patient's neurologic condition and influence the rate of sodium correction.

Prior to establishing a diagnosis of SIADH, a detailed history should be obtained in order to exclude the numerous disorders
capable of causing hyponatremia (see Causes).
Physical

On physical examination, evaluation of volume status is important. SIADH is characterized by euvolemic hyponatremia. Edema
in a hyponatremic patient is inconsistent with SIADH and may represent another hyponatremic states such as CHF, cirrhosis, or
nephrotic syndrome. Prominent physical examination findings may be seen only in severe or rapid-onset hyponatremia and
include confusion, lethargy, weakness, myoclonus, asterixis, depressed reflexes, generalized seizures, ataxia, nystagmus,
tremor, dysarthria, dysphagia, and coma.
Causes
Causes

Causes of syndrome of inappropriate antidiuretic hormone secretion (SIADH) vary widely. The syndrome was first
described in patients with bronchogenic carcinoma. SIADH may be a marker for occult malignancy such as head and
neck cancers. SIADH may also be manifested in cases of hypothyroidism and is corrected when thyroid hormone is
replaced.

Many therapeutic agents can induce SIADH. Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin
E2, which modulates vasopressin action and can result in decreased water excretion.5 SIADH has been reported as
an adverse effect of multiple psychotropic medications.14,15 While the exact mechanism of action is unknown, it
has been proposed that serotonin and serotonergic medications cause increased ADH secretion via the 5-HT1C and
5-HT2 receptors.15

SIADH should be differentiated from hospital-acquired hyponatremia often seen secondary to overzealous
administration of hypotonic IV fluids.6

Some of the causes of SIADH are listed below:

Central nervous system disease - Tumor, trauma, infection, cerebrovascular accident, subarachnoid hemorrhage,
Guillain-Barré syndrome, delirium tremens, multiple sclerosis
Pulmonary disease - Tumor, pneumonia, chronic obstructive pulmonary disease, lung abscess, tuberculosis, cystis
fibrosis, positive-pressure ventilation
Carcinoma -Lung, pancreas, thymoma, ovary, lymphoma
Drugs - Exogenous vasopressin, nonsteroidal anti-inflammatory drugs, nicotine, diuretics, chlorpropamide,
carbamazepine, tricyclic antidepressants, SSRIs, vincristine, thioridazine, cyclophosphamide, clofibrate,
bromocriptine, haloperidol, thiothixene, exogenous oxytocin, MAOIs
Surgery - Postoperative
Idiopathic